Acute Nursing Certification Program

Transcription

1 NEO Stroke Network s Acute Nursing Certification Program Level ONE

2 NEO Stroke Network s Acute Nursing Certification Program Launched at Hôpital régional de Sudbury Regional Hospital in the summer and fall of 2010, this program is a regional initiative made available to medical nursing units in the North East for use as a nursing certification Self Learning Program. The program is currently available as a paper copy in a binder that includes all text, pictures, diagrams, tests, references and appendices. In the future, a paperless, online copy will be available for those nurses who choose to complete this program on a work or personal computer. The program consists of eight Stroke Care Topics that can be completed in any order and are arranged as separate modules, each with its own quiz. Each module should take 45 minutes to 75 minutes to complete depending on the module and the nurse s background/experience. A score of 80% is considered a passing score. Although the answer key will not be posted, it is acceptable that the quizzes be done with an open book. Once initiated, the nurse will be given a set amount of time as determined by the manager to complete all eight modules. The Nurse Clinician of the unit or a designate will be the official monitor and tracker of the certification program, accepting and marking all the quizzes and issuing Certificates of Completion to each nurse. The Nursing Certification Program consists of three distinct levels of certification. Level one is includes eight modules, which are: 1) Neuroanatomy, Pathophysiology and Classification of Stroke 2) Pre-hospital and Emergency Management 3) Diagnostics and Assessments 4) Acute Stroke Management 5) NIHSS Training 6) Swallowing, Feeding and Oral Care 7) Mobility and Positioning for the Stroke Patient (incl the DVD) 8) Secondary Stroke Prevention Level two is highly desired for all nurses working in acute stroke care as it is consistent with best practice. It includes training for and certification in an evidenced-based

3 Swallowing Screen Tool. An example of one is TOR-BSST. Your centre may not have implemented a tool at this time. At Sudbury Regional Hospital, TOR-BSST training is currently organized by the Speech Language Pathologist whereby the nurse participates in a four hour training session and is observed completing two skilled TOR-BSST screens on stroke patients. Level three is completion of Apex Innovation s Hemisphere s Stroke Competency e- learning series. This is a new multi-level; interactive; comprehensive; web based educational series from pre-hospital stroke management to emergency care to acute care. It has been designed to train all levels of users, from students to physicians. It has a very comprehensive module on neuroanatomy and pathophysiology of stroke. Registered users receive a key which acts as a one year license to participate in the online series. Users can take as much time as desired to complete each module as long as all modules are successfully completed at the one year mark. The fee for this key will be reimbursed to the nurse once he/she has shown their Certificate of Completion for the series to the Nurse Clinician or designate. Staying current Each nurse is required to re-certify every two years by completing Level one again and demonstrating a score of 80% or better on each of the module s quizzes. The content in the binder (and electronic version) will be reviewed annually and updated according to current Canadian Best Practice Recommendations for Stroke Care and other evidence-based guidelines relevant to the content.

4 NEO Stroke Network s Acute Nursing Certification Program TABLE OF CONTENTS 1. Acute Nursing Certification Program Description and Process 2. Table of Contents 3. MODULE ONE Pathophysiology of Stroke, Neuroanatomy, Stroke Syndromes i) Classification of Stroke ii) Etiology iii) Brain Anatomy iv) Blood Supply v) Stroke Syndromes vi) References vii) Module One Quiz 4. MODULE TWO Pre-Hospital Care and Emergency Management i) Warning Signs of Stroke ii) Emergency Medical Services iii) Acute Thrombolytic Therapy iv) Adverse Effects of t-pa (Alteplase) v) Stroke Mimics vi) Acute ASA Therapy vii) Reducing Ischemic Damage from Hypertension, Hyperglycemia, Hyperthermia, O2 de-saturation viii) References ix) Module Two Quiz 5. MODULE THREE Diagnostics and Assessments i) Acute Nursing Assessment ii) Standardized Neurological Assessments (CNS, NIHSS, GCS) iii) Other Assessments

5 iv) Investigations v) References vi) Module Three Quiz 6. MODULE FOUR Acute Stroke Management i) Stroke Unit ii) The Team of Professionals iii) Post Stroke Complications iv) Other Effects of Stroke v) Discharge Planning vi) References vii) Module Four Quiz 7. MODULE FIVE NIHSS Training OR CNS Training 8. MODULE SIX Swallowing, Feeding and Oral Care i) Dysphagia Facts ii) Normal Swallow iii) Aspiration iv) Dysphagia Screening v) Dysphagia Diets vi) Feeding Strategies vii) Indications for Enteral Nutrition viii) Oral Care ix) References x) Module Six Quiz 9. MODULE SEVEN Mobility and Positioning Educational DVD (to be available soon) i) Considerations ii) General Principles When Assisting a Stroke Survivor iii) Preventing Injury to the Stroke Survivor and You iv) Hemiplegic Shoulder v) Aids and Equipment vi) Positioning Techniques vii) Mobilizing Techniques Including Transfers viii) DVD: Mobilizing and Positioning a Stroke Survivor ix) References x) Module Seven Quiz

6 10. MODULE EIGHT Secondary Stroke Prevention i) Primary Prevention ii) Lifestyle Modification iii) Medication Management iv) Carotid Intervention v) Transient Ischemic Attack (TIA) vi) Secondary Prevention Clinic vii) Patient Teaching re: Medications v) References v) Module Eight Quiz 11. Hospital - Specific Chart Forms (content will vary for each centre) 12. Other Resources i) Northeastern Ontario Stroke Network (NEOSN) Info sheet ii) EVERYTHING STROKE at your fingertips: an Electronic Toolkit for Health Care Providers (announcement) iii) Stroke Organizations: Lists and Websites iv) NEOSN Professional Education Fund 13. APPENDICES i) How to Obtain Level Two Certification ii) How to Obtain Level Three Certification with Apex Innovations Hemisphere s Stroke Competency Series 14. Acknowledgements 15. Certificate of Completion of LEVEL ONE and Pre and Post Self-Evaluation/Feedback/ Comment Form

7 NEO Stroke Network s Acute Nursing Certification Program LEARNING OBJECTIVES MODULE ONE Pathophysiology of Stroke Neuroanatomy Stroke Syndromes Upon completion of this module, nurses will be able to define and/or describe: Types of Stroke Etiology of Stroke General Brain Anatomy Major Blood Vessels of Cerebral Circulation Common Stroke Syndromes Right Sided Clinical Deficits Left Sided Clinical Deficits

8 MODULE ONE The following content is from the Acute Stroke Management Resource, Heart and Stroke Foundation of Ontario, Anatomy and Physiology workshop package. It has been edited and formatted for the NEO Stroke Network Self Learning Package

9 Pathophysiology and Anatomy of Stroke Ischemic stroke 80% of all strokes are caused by blockage of an artery resulting in diminished blood flow Usually the result of a blood clot, either thrombotic or embolic in nature Blockage may also occur because of progressive blood vessel occlusion, due to atherosclerosis, or because of local high pressure collapse of small blood vessels Approximately 50% of ischemic strokes are due to a thrombosis Of that 50%, 30% are related to large-vessel disease, especially of the carotid, middle cerebral, or basilar arteries 20% are related to small vessel disease of the deep penetrating arteries, such as the lenticulostriate, basilar penetrating, and medullary arteries (these are known as lacunar infarcts) The remaining 30% of ischemic strokes are embolic 1

10 Medical Illustration 2010 Nucleus Medical Media, Inc. Clot stops blood supply to an area of the brain Etiology of Ischemic Stroke The cause of ischemic stroke can be further classified as one of the following: 1. Large vessel disease may be classified as: a) Cardioembolism - often a result of atrial fibrillation or left ventricular damage after myocardial infarction b) Atherosclerosis - causes a progressive narrowing of the blood vessel through deposit of plaque on the arterial wall. 2. Small vessel disease, known as lacunar infarct, is thought to be the result of occlusion of single, small perforating arteries, located deep in the subcortical areas of the brain. Hypertension is thought to be a major risk factor associated with lacunar infarcts. 2

11 3. Cryptogenic strokes are strokes with no identified cause or etiology. Cryptogenic strokes are more commonly found in younger population, <45years. (Ionita et al., 2005) The classic risk factors for stroke are usually absent in cryptogenic stroke patients. However, Ionita et al (2005) reported that echocardiography studies in these stroke patients showed an increase incidence of Patent Foramen Ovale (PFO) in up to 45% of cases. Hemorrhagic stroke Caused by arterial rupture Can damage other brain tissue as a result of increased intracranial pressure and compression of brain tissue 20% of all strokes 10% of are due to intracerebral hemorrhage 10% are due to subarachnoid hemorrhage or bleeding from AVM (arteriovenous malformation) Medical Illustration 2010 Nucleus Medical Media, Inc. Hemorrhage/blood leaks into brain tissue 3

12 Etiology of Intracerebral Hemorrhage: 1. PRIMARY hemorrhage Hypertension is responsible for approximately 75% of all cases of primary Intracerebral Hemorrhage (ICH). Cerebral amyloid angiopathy (a disease of small blood vessels in the brain with deposits of amyloid protein which may lead to stroke, brain hemorrhage or dementia) is also a common cause. The use of fibrinolytics and anticoagulants make up approximately 10% of all ICH. (Manno et al, 2005) Drug abuse may cause sudden and severe elevations in blood pressure resulting in ICH. Image courtesy of Alberta Health Services 4

13 2. SECONDARY hemorrhage Underlying vascular abnormalities such as aneurysm, arteriovenous malformation are causes of secondary ICH, which makes up approximately 5 % of all ICH. Hemorrhagic transformation, secondary bleeding into the infarcted site, is considered by some to be a natural evolution of a stroke and some studies suggest that almost all infarcts have some element of petechial hemorrhage. Hemorrhagic transformation may be influenced by the size, location and cause of the stroke. The use of antithrombotics including anticoagulants and thrombolytics increases the likelihood of hemorrhagic transformation. Cerebrum The cerebrum is the largest portion of the brain and contains 2 hemispheres. The left hemisphere controls the right side of the body and the right hemisphere controls the left side of the body. The two hemispheres are joined by the corpus callosum. Permission granted to use image 5

14 In 97% of the population, the left hemisphere is the dominant hemisphere. Cerebral Cortex is divided into 4 lobes: Frontal Parietal Temporal Occipital Two important structures are found in the frontal and parietal lobes. In the posterior portion of the frontal lobe, the primary motor cortex can be found. This is also referred to as the motor strip and is involved in the ability of the body to move various body parts. Damage to parts of the motor strip may result in symptoms such as paralysis of the face, arm or leg or difficulty speaking. In the anterior part of the parietal lobe is the primary sensory cortex or sensory strip. It corresponds directly to the body part locations of the motor strip and is involved in the ability to feel or recognize textures. 6

15 Blood Supply to the Brain Arterial supply is from carotid and vertebral arteries which begin extracranially Internal carotid arteries supply anterior 2/3 of hemispheres Vertebral and basilar arteries supply posterior and medial regions of hemispheres, brainstem, diencephalon, cerebellum; cervical spinal cord Both the carotid (anterior) and vertebral (posterior) blood supply originates outside of the cranium from the internal carotid arteries. The carotid and vertebral arteries enter the cranial cavity via the internal carotid, which come off the common carotids and vertebral arteries which originate from the subclavian arteries. 7

16 The internal carotid arteries and its branches supply 2/3 of the cerebral hemispheres. The anterior circulation s major blood vessels are the anterior cerebral and the middle cerebral arteries. The posterior circulation s major vessels are the vertebral, basilar and posterior cerebral arteries and supply the medial and posterior sections of the hemispheres, the brainstem, deep brain structures such as the diencephalon, the cerebellum and the cervical section of the spinal cord. Circle of Willis An important structure within the cerebral circulation is the Circle of Willis. It is located at the base of the brain. The primary purpose of the Circle of Willis is to provide multiple paths of oxygenated blood to the brain. If any of the major vessels become occluded, the various paths of the Circle of Willis attempt to ensure circulation is maintained. 8

17 The Circle of Willis is comprised of the following vessels: Anterior Cerebral Artery Middle Cerebral Artery Anterior Circulation Anterior Communicating Artery Posterior Cerebral Artery Posterior Communicating Artery Posterior Circulation The Posterior and Anterior Communicating Arteries are responsible for connecting the right and left side blood vessels so that circulation is seamless. Major Cerebral Arteries Image courtesy of Communications, Alberta Health Services 9

18 The Anterior Cerebral Artery (ACA) originates from the internal carotid artery and supplies the anterior portion of the basal ganglia, the corpus callosum, the medial and superior portions of the frontal lobe and the anterior part of the parietal lobe. Region of Anterior Cerebral Artery Permission granted to use image Legend for picture: Anterior Cerebral Artery- blue Middle Cerebral Artery- pink Posterior Cerebral Artery- green The key functional areas that receive blood supply from the anterior cerebral artery are: Primary motor cortex involving the leg and foot areas The centre for micturation found in the frontal lobe The motor planning centre found in the frontal lobe The anterior and middle portions of the corpus callosum A patient who has a stroke involving the anterior cerebral artery may experience weakness in the leg and foot, difficulties with micturation, difficulties with the ability to plan and carry out tasks such as dressing. 10

19 The Middle Cerebral Artery (MCA) arises from the internal carotid artery. Region of Middle Cerebral Artery Permission granted to use image Legend for picture: Anterior cerebral artery-blue Middle cerebral artery- pink Posterior cerebral artery- green The middle cerebral artery is the largest of the major vessels and supplies blood to over 2/3 of the cerebrum. The MCA has 3 branches and passes laterally under the frontal lobe and between the temporal and frontal lobes. The M1 segment is also referred to as lentriculostriate arteries and are located in the deeper sections of the brain called the basal ganglia and most of the internal capsule. 11

20 These lentriculostriate vessels are small vessels located deep in the brain and are also a common site for small vessel or lacunar strokes. The superior branch of the MCA supplies the lateral and inferior frontal lobe and anterior parts of the parietal lobe. The inferior branch of the MCA supplies the lateral temporal lobe, the posterior parietal lobe and the lateral occipital lobe. The Posterior Cerebral Artery (PCA) is responsible for the blood supply for midbrain, hypothalamus and thalamus, posterior medial parietal lobe, corpus callosum, inferior and medial temporal lobe and inferior occipital lobe. Key Functional Areas that receive blood supply from the PCA are: Primary visual cortex in the occipital lobe 3rd cranial nerve in the midbrain Sensory control Hypothalamus-body temperature control, hunger, thirst, hormone release (Antidiuretic hormone) Thalamus-relaying messages to cortex, level of arousal, awareness, pain Communication between the hemispheres Region of Posterior Cerebral Artery Permission granted to use image 12

21 Legend for picture: Anterior Cerebral Artery- blue Middle Cerebral Artery- pink Posterior Cerebral Artery- green Patients who experience a stroke in the Posterior Cerebral Artery may present with symptoms such as problems with recognizing objects, visual disturbances, drooping eyelid, inability to move the eye in, up & out, down & out, difficulty maintaining body temperature, abnormal hormone responses, coma, hyperesthesia Cerebellum The cerebellum has its own major blood vessels which originate from the vertebrobasilar vessels. The 3 cerebellar vessels are: Superior Cerebellar Anterior Inferior Cerebellar Posterior Inferior Cerebellar The major functions of the cerebellum are control of fine motor movement, coordination of muscle groups and maintaining balance and equilibrium. Permission granted to use image 13

22 There are 2 syndromes often seen with cerebellar strokes: 1. Lateral pontine syndrome Involves basilar and anterior inferior cerebellar artery Symptoms: ipsilateral ataxia of arm and leg, contralateral weakness of upper and lower extremities, contralateral hemisensory loss - pain and temperature 2. Lateral Medullary Syndrome (Wallenberg Syndrome) Involves distal and superior medullary artery branches of vertebral artery and the posterior inferior cerebellar artery Symptoms: Ipsilateral sensory loss-face-pain and temperature, ipsilateral ataxia of arm and leg, gait ataxia, nystagmus, nausea and vomiting, vertigo, hoarseness, dysphagia, contrateral hemisensory loss-pain and temperature, horner syndrome (constricted pupil, partial ptosis, loss of hemifacial sweating), hiccoughs Brain Stem The brain stem receives its blood supply from the posterior cerebral artery and the vertebrobasilar vessels. 14

23 The brain stem is divided into 3 major sections: Midbrain: major functions include involvement in vision, hearing, eye movement and body movement Pons: involved in motor control and sensory analysis, level of consciousness, sleep Medulla: responsible for maintaining vital body functions such as breathing and heart rate One of the major structures housed in the brain stem are the cranial nerves. While there are 12 cranial nerves, Cranial nerves 1& ll originate in the frontal lobe and will not be discussed in this section. Cranial nerves lll-xll originate in the brain stem. Patients that experience a stroke in the brain stem will present with symptoms that involve cranial nerve functions such as swallowing, eye movements, facial expression and tongue movements. The brain stem serves an important role as a pathway between the spinal cord and the brain. The afferent and efferent pathways run through the spinal cord and connect with brain centres for interpretation and response to stimuli. The Reticular Activating System originates in the brain stem and is responsible for our wakefulness and attention. It is a very sensitive system that spans the brain and reacts to interruptions in its ability to work. An expanding stroke will interrupt its ability to keep the patient awake, resulting in the patient presenting with a decreased level of consciousness. Patients who experience a brain stem stroke may present with any of the following: Decreased level of consciousness Ipsilateral lower motor neuron facial weakness or sensory loss Contralateral hemiparesis Pupillary changes Hiccoughs, vertigo Bilateral motor findings Diplopia, gaze palsies, intranuclear opthalmoplegia Dysphagia 15

24 Dysarthria Ataxia Collateral Circulation Collateral circulation is an important feature of the brain and for stroke patients. Not all blood vessels have the capability to be able to create collateral circulation. Vessels such as the lenticulostriate vessels are terminal vessels which do not connect with other vessels. Therefore, vessels associated with the lenticulostriate vessels that become occluded will become ischemic. However, there are vessels that can connect or anastomose with other vessels, creating a redundancy that can permit collateral circulation when one vessel is blocked. These vessels include: External and internal carotid via branches of the opthalmic artery Major intracranial vessels via the Circle of Willis Small cortical branches of the anterior cerebral, middle cerebral and posterior cerebral and cerebellar arteries Some stroke may go unnoticed as the collateral circulation has taken over the function of supplying an area of the brain Thanks to the Circle of Willis, by design, the anterior circulation is connected to the posterior circulation 16

25 Ischemic Stroke: Carotid Syndromes The carotid arteries and their branches, the anterior and middle cerebral arteries, form the anterior circulation and the vertebral, basilar, posterior cerebral arteries and their branches form the posterior circulation. Clinical stroke syndromes depend on the area of the cerebral circulation disrupted. Typically, the anterior or carotid circulation stroke syndromes present with symptoms that include sensory or motor deficits aphasia cortical sensory loss apraxia or neglect visual field deficits or retinal ischemia Ischemic Stroke: Vertebrobasilar Syndrome Strokes affecting the posterior circulation or vertebrobasilar system, present with symptoms such as Diplopia Vertigo Coma at onset Crossed sensory loss Bilateral motor signs Isolated field defect Pure motor and sensory deficit Dysarthria Dysphagia Ischemic Stroke: Lacunar Syndromes Makes up 25% of all ischemic strokes Presumed to be occlusion of single small perforating artery Predominantly in the deep white matter, basal ganglia, pons 17

26 Blood vessel: lenticulostriate branches of the Anterior Cerebral and Middle Cerebral Arteries Lacunar infarction results from infarction of one of the lenticulostriate vessels, the penetrating branches of the circle of Willis, the MCA stem, or vertebral or basilar arteries. Type of Syndrome Patient Presentation Pure motor hemiparesis Results from an infarct in the internal capsule or pons Contralateral Hemiparesis of face, arm and leg, dysarthria Contralateral motor hemiparesis with motor aphasia Results from an infarct of the left frontal area with cortical involvement Ataxic hemiparesis Results from an infarct in the pons Hemiparesis of face, arm and leg with inability to speak Paresis of the contralateral leg and side of the face, ataxia of the contralateral leg and arm 18

27 Dysarthria and clumsy hand syndrome Results from an infarct in the pons or internal capsule Pure sensory stroke Results from an infarct in the thalamus Dysarthria, dysphagia, contralateral facial and tongue weakness, paresis and clumsiness of the contralateral arm and hand Contralateral sensory loss to all modalities that usually affect the face, upper and lower extremities May be painful Kistler JP, Ropper AH, Martin JB. Cerebrovascular diseases. In: Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL, eds. Harrison s Principles of Internal Medicine. 13th ed. New York: McGraw Hill; 1994: Fisher,CM. (1991). Lacunar Syndromes, 1, Ischemic Stroke: Left (dominant) Hemisphere Stroke The CT scan shows a large area of infarction in the territory of the left middle cerebral artery. The MCA is the artery most often occluded in ischemic stroke. 19

28 The associated neurological signs and symptoms form a common pattern of stroke presentation involving the left, or dominant, hemisphere. Aphasia Right field defect Left gaze preference Right upper motor neuron facial weakness Right hemiparesis Right hemisensory loss Ischemic Stroke: Right (non-dominant) Hemisphere Stroke The CT scan shows a large area of infarction in the territory of the right middle cerebral artery. 20

29 The associated neurological signs and symptoms form a common pattern of stroke presentation involving the right, or non-dominant, hemisphere. Left neglect, inattention Left field defect Right gaze preference Left upper motor neuron facial weakness Left hemiparesis Left hemisensory loss, sensory extinction Ischemic Stroke: Cerebellar Infarct The MRI scan shows an area of ischemia in the left cerebellum. This stroke presentation should be considered a neurological emergency because of the possible risk of raised intracranial pressure due to compression of the fourth ventricle. 21

30 The following associated signs and symptoms form a common pattern of stroke presentation involving the cerebellum. Headache, nausea/vomiting Vertigo, imbalance Normal tone, power, reflexes Inability to sit or stand Ataxia or loss of normal coordination Late signs: Decreasing level of consciousness Diplopia, gaze palsy Ipsilateral V, Vll impairment Ischemic Stroke: Brainstem Stroke This MRI scan shows an area of ischemia in the right pons, in the brainstem 22

31 The following associated neurological signs and symptoms form a common pattern of stroke presentation involving the brainstem. Decreased LOC Crossed findings Ipsilateral lower motor neuron facial weakness or sensory loss AND contralateral hemiparesis Pupillary changes Hiccoughs, vertigo Bilateral motor findings Diplopia, gaze palsies, intranuclear opthalmoplegia Dysphagia Dysarthria Ataxia 23

32 The Brain and Function How Stroke Affects Function A stroke is a loss of function that results from the blood supply to the brain being cut off. The following describe how a stroke affects the function of different areas of the brain: Frontal Lobe Arm, opposite side of stroke Leg, opposite side of Frontal stroke Judgment, personality, lobe attention Speaking and writing if stroke is on the dominant side Parietal lobe Parietal Lobe Arm, opposite side of stroke Leg, opposite side of stroke Sensation of touch Visual and sensory perception, if stroke is on the non-dominant side Temporal Lobe Sense of smell Temporal Memory lobe Understanding spoken and written language and math skills if stroke is on the dominant side (part of the Parietal lobe as well) Brain Brainstem Stem Breathing Modulation of temperature and blood pressure Swallowing Cerebellum Cerebellum Coordination Balance Occipital lobe Occipital Lobe Vision Blood Supply and the Brain The Anterior Cerebral Artery supplies blood to the medial (central) parts of the Frontal and Parietal Lobes. The Middle Cerebral Artery supplies blood to the lateral (outer) parts of the Frontal and Parietal Lobes and the Temporal Lobe. The Middle Cerebral Artery is the most common site of stroke. The Posterior Cerebral Artery and Vertebro-Basilar Artery systems supply blood to the Cerebellum, Brain Stem, Occipital Lobe, and the posterior (back) part of the Temporal Lobe. Anterior Cerebral Artery Middle Cerebral Artery Posterior Cerebral Artery Opthalmic Artery Cerebellar Arteries Internal Carotid Artery Basilar Artery Vertebral Artery

33 Module One Pathophysiology of Stroke, Neuroanatomy, Stroke Syndromes REFERENCES The main source for this module was: Acute Stroke Management Resource. (2007). Heart and Stroke Foundation of Ontario, Anatomy and Physiology of Acute Stroke power point presentation. Retrieved from Eng lish.htm That presentation listed the following sources for the content: American Association of Neuroscience Nurses American Stroke Association Brain Attack Coalition Canadian Hypertension Education Program Canadian Stroke Strategy European Stroke Initiative Heart and Stroke Foundation Prof Ed Heart and Stroke Foundation of Canada Internet Stroke Centre National Institute of Neurological Disorders and Stroke

34 Scottish Intercollegiate Guidelines Network StrokeEngine

35 NEO Stroke Network s Nursing Certification Program MODULE ONE Pathophysiology of Stroke Neuroanatomy Stroke Syndromes Quiz You may use your binder as a reference to answer these questions Submit your completed quiz to the Nurse Clinician or designate for marking Your test will be returned to you to keep in your binder NEO Stroke Network Developed April 2010

36 DATE: NAME: 1. The etiology of ischemic stroke can be classified as a. Large vessel b. Small vessel c. Cryptogenic d. all of the above 2. The Cerebrum is made up of all but one of the following structures. Select the structure not part of the cerebrum. a. Temporal lobes b. Occipital lobes c. Parietal lobes d. Superior and inferior cerebellar lobes 3. Hemorrhagic transformation, or secondary bleeding into an infarcted lesion, is often considered to be a natural evolution of an ischemic stroke. It can be serious clinically if there is bleeding beyond the original territory or if mass effect occurs. It is influenced by the a. Size of the stroke b. Location of the stroke c. Etiology of the stroke d. All of the above 4. The three main branches of the Internal Carotid Artery: the Anterior Cerebral Artery (ACA), Middle Cerebral Artery (MCA) and Anterior Communicating Artery together form the a. Posterior circulation b. Circle of Willis c. Anterior circulation d. Cerebellar circulation

37 5. Collateral Circulation can occur because of the: a. Redundancy in our cerebral vasculature b. The Circle of Willis c. Terminal vessels d. Both Answer A and B 6. Small vessel disease causing stroke is thought to be the result of occlusion of single, small penetrating arteries deep in the brain. These strokes are called: a. Cerebellar strokes b. Lacunar strokes c. Cryptogenic strokes d. Arteriovenous malformations 7. Cerebellar infarct may present with all but one of these signs: (Choose the exception) a. Impaired executive functioning; decision making b. Vertigo,imbalance c. Ataxia or loss of normal coordination d. Diplopia 8. The brainstem is responsible for a. Understanding written language b. Perception of the surrounding environment c. Autonomic functions ie. respiration, blood pressure, heart rate d. Thoughts and behaviour TRUE/FALSE Questions (CIRCLE the correct letter) T F 1. The left hemisphere controls the right side of the body AND is most often where the language center is located.

38 T F T F T F T F 2. The cerebellum is responsible for sensation, vision and memory. 3. The middle cerebral artery has a large territory and is most often the artery occluded in stroke. 4. Lacunar syndrome is commonly referred to as a pure motor stroke presenting with contralateral hemiparesis. 5. Tumour or a brain abscess may present like a stroke and is considered to be one of the so-called Stroke Mimics. SCORE: / 13 Stroke Unit/Medical Unit Nurse Clinician/Designate (signature)

39 NEO Stroke Network s Acute Nursing Certification Program LEARNING OBJECTIVES MODULE TWO Pre-Hospital and Emergency Management Upon completion of this module, nurses will be able to: State the Warning Signs of Stroke Understand the Role of EMS in Hyperacute Stroke Explain Thrombolytic Therapy - and the importance of quick assessment and administration within the time window Identify Stroke Mimics Understand Acute ASA Therapy Explain the Contributing Factors to Ischemic Damage

40 NEO Stroke Network s Acute Nursing Certification Program MODULE TWO Pre-hospital Care and Emergency Management Self Learning Program NEO Stroke Network Developed April 2010

41 Pre-hospital Care and Emergency Management Warning Signs of Stroke Sudden onset of: Weakness or numbness Speech disturbances Unexplained dizziness Visual changes Sudden severe headache of unknown cause Emergency Medical Services Hyperacute Stroke is defined as the health care activities that take place from the time of first contact between a potential stroke patient and medical care. This period ceases once the patient is either admitted to hospital or discharged back into the community. Patients who show signs and symptoms of hyperacute stroke in the community must be treated as time-sensitive emergency cases and should be transported without delay to the closest institution that provides emergency stroke care. Immediate contact with emergency services by patients or members of the public is strongly recommended because it reduces time to treatment for acute stroke. EMS service dispatchers must triage patients showing signs of hyperacute stroke as a priority dispatch. EMS providers should be using a standardized screening tool. EMS implemented a newly revised Paramedic Prompt Card. The prompt card assists EMS providers in, first, recognizing the signs and symptoms of stroke and second, in decision making around the most appropriate hospital to which to transport the patient. 2

42 Paramedic Bypass Protocols exist in each region whereby the EMS providers will bypass the local community hospital and transport the patient, up to 2 hours in the ambulance, to access a centre equipped to provide optimal acute stroke treatment, and arrive within 3.5 hours from the time of stroke onset. The 2008 Canadian Best Practice Recommendations for Stroke Care also emphasize the need for rapid transport of acute stroke patients to appropriate facilities but unfortunately lack of public awareness of stroke signs and symptoms AND lack of knowledge that stroke is an emergency still exists. PARAMEDIC PROMPT CARD FOR ACUTE STROKE PROTOCOL Indications for Patient Redirect or Transport to a Designated Stroke Centre Redirect or transport to a Designated Stroke Centre will be considered for patients who: Present with a new onset of at least one of the following symptoms suggestive of the onset of an acute ischemic stroke: unilateral arm/leg weakness or drift slurred speech or inappropriate words or mute unilateral facial droop AND Can be transported to arrive at a Designated Stroke Centre within 3.5 hours of a clearly determined time of symptom onset or the time the patient was last seen in a usual state of health. NOTES: 1. A Designated Stroke Centre is a Regional Stroke Centre, District Stroke Centre or Telestroke Centre. 2. Patients will be redirected or transported to the closest Designated Stroke Centre. 3. Patients whose symptoms improve significantly or resolve during transport will continue to a Designated Stroke Centre 4. Out-of-hospital transport will not exceed two hours. Exclusions for Patient Redirect to a Designated Stroke Centre Any of the following conditions exclude a patient from being redirected to a Designated Stroke Centre: CTAS Level 1 and/or uncorrected Airway, Breathing or Circulation problem Patients whose symptoms have resolved prior to paramedic assessment Blood sugar < 3.0mmol/l Seizure at onset of symptoms or observed by paramedic Glasgow Coma Scale <10 CACC will authorize the transport once notified of the patient's need for redirect under the Stroke Protocol. 3

43 Acute Thrombolytic Therapy All patients with disabling acute ischemic stroke who can be treated within 4.5 hours after symptom onset should be evaluated without delay to determine their eligibility for treatment with t-pa (Alteplase). Eligible patients are those who can receive t-pa within 4.5 hours of the onset of stroke symptoms in accordance with criteria adapted from the National Institute of Neurological Disorders and Stroke tpa Stroke Study and Third European Cooperative Acute Stroke Study (ECASS III). The introduction of thrombolytic therapy has provided a proven treatment for acute ischemic stroke patients if given as soon as possible and within the time window. However, it is a high risk treatment that should only be given by personnel trained in its use, in a centre equipped to investigate and monitor patients appropriately. Goal of thrombolytic therapy is to limit irreversible ischemic damage caused by an arterial occlusion. Thrombolysis will promote reperfusion of the viable tissue of the penumbra, improving stroke prognosis and outcome. It is important to note that time is brain and the closer to the time of stroke onset that reperfusion occurs, the better the patient prognosis. What is Tissue Plasminogen Activator (t-pa or Alteplase)? As excerpted from Faaast FAQs for Nurses, page 7, Heart and Stroke Foundation of Ontario (2007)....t-PA (Alteplase) is a thrombotic agent (clot-busting drug) that can destroy an existing blood clot that is approved for use in select patients having an ischemic stroke. It is to be given within the time window of 4.5 hours from last seen normal. Prior to administration of the drug, the patient must undergo specific diagnostic procedures to determine if there is any hemorrhage. This requires immediate access to CT scan imaging and blood work. 4

44 Administration is most often administered intravenously or sometimes intraarterially directly to the site of the clot via catheter, allowing for a greater dose of the drug with fewer potential side effects. What is the usual process prior to a patient receiving t-pa (Alteplase)? Ascertain time of onset (<than 4.5 hours) History and physical symptoms consistent with acute ischemic stroke CT to rule out hemorrhage stroke [or other etiology] CBC, platelets, lytes, glucose, INR, PTT etc Assessment by a Stroke Physician What are the major inclusion criteria for t-pa (Alteplase)? Ischemic stroke Clearly definable time of onset t-pa can be administered within 4.5 hours of symptom onset Symptoms present more than 1 hour without signs of resolution What are some absolute contraindications for t-pa (Alteplase)? TIA or stroke with rapidly improving deficit Hemorrhagic stroke BP>185/110 that does not respond to treatment Major surgery or trauma within 14 days Active internal bleeding or history of hematological abnormality or anticoagulation [this is dependent on INR value which may vary at across centres] Why work quickly to determine if t-pa (Alteplase) is the appropriate treatment? If thrombolysis takes place as soon as possible, the less brain tissue is affected. 5

45 Below you will see the infarcted tissue (ischemic core), the tissue that is still viable but lacking perfusion, therefore, at risk (ischemic penumbra), and the normal brain tissue. Normal brain tissue Brain tissue that is lacking perfusion, at risk of death Infarcted brain tissue NOTE: Our brain requires a constant uninterrupted supply of glucose and oxygen as the brain does not store glucose or oxygen. An interruption in either of these substances can lead to dysfunction. A complete interruption of blood supply to part of the brain for only 30 seconds can alter brain metabolism, for example, neuronal function may cease after 1 minute. After 5 minutes anoxia initiates a chain of events that may lead to death of brain tissue. Penumbra tissue remains viable for several hours after stroke. Penumbra cells are supplied by collateral arteries which contribute to reperfusion and thrombolytic therapy also works to perfuse the penumbra. A stroke patient should receive thrombolytic therapy as soon as possible but within a maximum of 60 minutes of arrival. A rapid and coordinated emergency department response to the arrival of a stroke patient facilitates early diagnosis and treatment. 6

46 The following maximum target times for emergency management of ischemic stroke have been established. Door-to-triage 1 minute Door-to-stroke team notification 5 minutes Door-to-CT scan 25 minutes Door-to-needle 60 minutes (The absolute and relative exclusion criteria for administration of t-pa and the t-pa Order Set are included in the Hospital-Specific Chart Forms section of those packages that are available at District Stroke Centres and Telestroke sites) There are adverse effects of t-pa to be aware of: Hemorrhage a) Superficial Bleeding Observe potential bleeding sites: venous & arterial puncture, lacerations, etc. Avoid invasive procedures during t-pa (Alteplase) and for 24 hours after (incl. N/G and foley catheter) Monitor all secretions for bleeding b) Intracranial hemorrhage Observe for deterioration of neuro status If suspected, stop t-pa (Alteplase) and notify M.D. Obtain CT scan and coagulation workup Angiodema a) Risk assessment Inquire if patient has had angioedema in past Take ACE inhibitor history Although angiotensin II (ATII) receptor antagonists have not been implicated in the angioedema reaction, caution is advised in patients reporting a history of ATII antagonist use 7

47 b) Monitoring Observe for facial, tongue, and/or pharyngeal angioedema 30 minutes, 45 minutes, 60 minutes and 75 minutes after initiation of IV t-pa infusion and periodically for 24 hours afterwards Stroke Mimics Not all cases that appear as a stroke are in fact a stroke. Be aware of the many other conditions that would be part of the differential diagnoses as they can present much like a stroke. Seizure Infection Hypoglycemia Syncope Brain abscess or tumour Drug overdose Head trauma Migraine Bell s palsy Hypertensive encephalopathy Acute ASA Therapy All acute stroke patients should be given at least 160mg of ASA immediately as a one time loading dose after brain imaging has excluded intracranial hemorrhage. [Evidence Level A] (ESO, NZ, RCP, SIGN 13). (Canadian Best practice Recommendations -2008) In patients treated with t-pa (Alteplase), ASA should be delayed until after the 24 hour post-thrombolysis scan has excluded intracranial hemorrhage. ASA ( mg daily) should then be continued indefinitely or until an alternative antithrombotic regime is started. In dysphagic patients, ASA may be given by enteral tube or by rectal suppository The administration of ASA in the hyperacute phase of stroke comes as a result of research that concluded that the administration of ASA within 48 hours of onset of presumed ischemic stroke reduces the risk of early recurrent ischemic stroke without a major risk of early hemorrhagic complications and improves long term outcomes. (Cochrane Database Systematic Review, 2007) 8

48 Goals of Acute Ischemic Stroke Management Reduce or minimize ischemic damage Reduce cerebral edema Prevent secondary complications Determine etiology of stroke Prevent recurrent stroke Facilitate access to rehabilitation and community reintegration Contributing Factors to Ischemic Damage While restoring blood flow to the penumbra is the goal of acute stroke management, there are multiple factors that should be considered and addressed as part of the management plan. Factors that play a role in contributing to potential increase in size of the infarct include: a) Blood pressure b) Blood glucose c) Body temperature d) Oxygen saturation It is important to assess and monitor vital signs to keep this goal at the forefront. from Heart & Stroke: Best Practice Guidelines for Stroke Care Acute Ischemic Stroke receiving t-pa Vital signs (including temperature) should be assessed as follows after beginning t-pa infusion: q 15 minutes for 2 hours q 30 minutes for 2 hours q 1hour for 6 hours q 4 hours for 14 hours 9

49 Acute Ischemic Stroke Non t-pa Vital signs (including temperature) should be assessed as follows: q 1 hour for 24 hours q 4 hours for 24 hours Or as indicated by hospital protocol a) Hypertension (HTN) Acute stroke patients often experience hypertension in the immediate hours after stroke onset. Elevated blood pressure may act as a compensatory mechanism to maintain cerebral perfusion. Normally, cerebral auto regulation maintains cerebral blood flow. However, as cerebral perfusion pressure decreases in the presence of stroke, normal auto regulation is lost and blood flow is dependant on the blood pressure There are many factors that cause hypertension secondary to stroke: full bladder, nausea, pain, pre existing hypertension, anxiety, a physiological response to hypoxia or increased intracranial pressure. The reason for lowering blood pressure is because HTN can increase cerebral edema, increase risk of hemorrhagic transformation, cause further vascular damage and stroke recurrence. There is a concern that reducing blood pressure too quickly and too low may cause neurological damage as a result of reduced perfusion pressure to the ischemic areas. Lowering of the blood pressure can result in serious consequences. Both hypertension and hypotension have been associated with poor patient outcomes. 10

50 For some stroke patients, blood pressure may decline spontaneously within the first few hours as a result of interventions such as moving the patient to a quieter area, emptying the bladder, allowing the patient to rest or controlling pain. Also, the treatment of increased intracranial pressure may result in a lowering of blood pressure. Blood Pressure Reduction BP reduction should be addressed cautiously Measure BP accurately, continuously monitor Clear data is lacking but: 2007 AHA/ASA Guidelines recommend: Initiate treatment if SBP>220mmHg or DBP>120mmHg t-pa candidates: Initiate treatment if SBP>185mmHG or DBP>110mmHG Lower blood pressure by 15-25% within 24 hours Medication selection on case by case basis but consider ability to lower blood pressure quickly but ability for rapid reversal NOTE The HRSRH non-t-pa Order Set adopted these guidelines: Hold antihypertensives x 24 hours unless SBP>220mmHg or DBP>120mmHg *Caution* - avoid rapid lowering of BP. If necessary treat with goal of reduction by ~ 15% within the first 24 hours NOTE Use of sublingual Nifedipine is contraindicated due to its prolonged effect and rapid decline in BP. 11

51 b) Blood Glucose - Hyperglycemia All patients with suspected acute stroke should have their blood glucose concentration checked immediately Blood glucose measurement should be repeated if the first value is abnormal or if the patient is known to have diabetes Markedly elevated blood glucose concentrations should be treated with glucose lowering agents immediately. (CSQCS, Australia) Hyperglycemia is associated with worse stroke outcomes and is also a risk factor for hemorrhagic transformation. It can also have a serious effect on aphasia, hemiparesis, and changes in mental status. It is unclear as to what extent post-stroke hyperglycemia is a normal physiological response or whether hyperglycemia increases cerebral damage. But studies have also shown that hyperglycemia is linked to an increased risk for in-hospital mortality in nondiabetic patients linked to an increased risk of a poor functional recovery Many stroke patients may not have known that they have diabetes (a modifiable risk factor) until admission to hospital. c) Body Temperature - Hyperthermia Increased body temperature (fever) in the setting of acute ischemic stroke is associated with poor neurological outcome (increased risk of morbidity and mortality), possibly secondary to increased metabolic demand, enhanced release of neurotransmitters, and increased free radical production. The source of any fever should be ascertained. The fever may be secondary to a cause of stroke, such as infective endocarditis, or may represent a complication such as pneumonia. (American Stroke Association, 2007) 12

52 d) Oxygen Saturation - Desaturation Ensuring adequate oxygenation of tissues is important in acute stroke management. Oxygen desaturation may exacerbate and worsen ischemic damage. Oxygen saturation should be monitored with the use of pulse oximetry and oxygen applied if oxygen saturation is <92%. (American Heart Association, 2007). Supplemental oxygen given to patients who are not hypoxic may result in the production of oxygen free radicals and contribute to worse outcome. Consideration and assessment of other causes of hypoxia should also be reviewed. These include pneumonia, partial airway obstruction, hypoventilation and atelectasis. Patients who have brain stem infarcts have the greatest risk of airway compromise due to impaired oropharyngeal mobility and loss of reflexes. 13

53 NEO Stroke Network s Acute Nursing Certification Program MODULE TWO Pre-Hospital and Emergency Management QUIZ You may use your binder as a reference to answer these questions Submit your completed quiz to the Nurse Clinician or designate for marking Your test will be returned to you to keep in your binder NEO Stroke Network Developed April 2010

54 DATE: NAME: 1. List the five warning signs of stroke: 5 points 2. The accepted time window to deliver the drug t-pa to a new stroke patient in our region is: a. 1.5 hours since last seen normal b. 4.5 hours since last seen normal c. 3.5 hours since last seen normal d. Within 24 hours of symptom onset 3. Adverse effects of t-pa to be aware of include: a. Bleeding b. Memory loss c. Angiodema d. Answer A and C 4. List three Stroke Mimics: 3 points 5. The following are contributing factors to ischemic damage except: (Choose the exception) a. blood pressure b. weakness c. oxygen saturation d. body temperature

55 6. All acute stroke patients should be given at least of ASA immediately as a one time loading dose: (fill in the blank) a. 160 mg b. 80 mg c. 325 mg d. 125 mg TRUE/FALSE Questions (CIRCLE the correct letter) T F T F T F 1. There are serious inclusion and exclusion criteria the physician MUST consider before determining if an acute stroke patient qualifies for thrombolytic therapy. 2. Blood Pressure reduction in the acute phase should be addressed cautiously and follow the guidelines of Hold antihypertensives x 24 hours unless SBP>220mmHg or DBP>120mmHg and avoid rapid lowering of BP. 3. Reduction of fever can wait till it has reached 38.5º C or beyond. SCORE: / 15 Stroke Unit/Medical Unit Nurse Clinician/Designate (signature)